It is now generally agreed that to achieve optimal glycemic control, patients with type 1 diabetes should be treated with intensive insulin therapy. This can be achieved by a continuous subcutaneous insulin infusion (CSII) or by multiple daily injections (MDI) using a combination of long-acting basal insulin (glargine or detemir) and a shortacting insulin (lispro, aspart, or glulisine) to control postprandial hyperglycemia. However, it remains controversial whether these two modalities are equally effective or if one is superior to the other. One meta-analysis 1 and the 5-nations trial 2 concluded that CSII resulted in better glycemic control compared to MDI. However, older insulins (neutral protamine Hagedorn or regular) and outdated pump technologies were used in these studies. Other studies have shown CSII to be equally effective 3 or CSII being superior 4 to MDI. Although a more recent meta-analysis also showed that the frequency of severe hypoglycemia in type 1 diabetes was reduced markedly in trials during CSII compared with MDI based on isophane and lente insulins, the authors acknowledged that they did not find any trials comparing CSII and MDI based on the newer long-acting insulin analogs where severe hypoglycemia could be analyzed. Moreover, their conclusions on hemoglobin A1c (HbA1c) were based on a relatively small number of trials concerning glargine and none using detemir. 5 In addition, it is not clear if one of these two treatment modalities is superior to the other in routine clinical practice.We therefore compared the degree of glycemic control achieved, frequency and severity of hypoglycemic episodes, and perception of quality of life achieved by CSII versus MDI in our practice. We sent letters inviting all patients being treated with CSII or MDI in our practice that had been followed for at least 2 years-113 letters were sent to pump patients and 137 to patients on MDI. Fifty-three patients treated with CSII using insulin lispro or aspart and 54 patients treated with MDI therapy (glargine and either insulin lispro or aspart) agreed to participate. Hypoglycemic episodes were self-reported as mild or severe (requiring third-party help). Life satisfaction, impact, and worry related to diabetes were assessed by the diabetes quality of life questionnaire. 6The patient demographics and results of the study are shown in Table 1.The mean HbA1c was significantly lower in the CSII group. Episodes of severe hypoglycemia were less frequent, and overall satisfaction was greater in the CSII group compared to the MDI group. These findings are similar to those seen in randomized controlled trials.

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3324 A daily aspirin in patients with myocardial infarctions (MI) effectively reduces the risk of occlusive vascular disease by 25%. This protective effect is reduced or absent in diabetics possibly because aspirin induced inhibition of platelet function is diminished. We tested the hypothesis that the amount of aspirin induced inhibition of platelets in diabetics is decreased. Methods: Each subject was evaluated at 2 time points: off-aspirin and 2-hours after observed ingestion of a 325mg aspirin tablet. Platelets were stimulated in a light aggregometer with platelet prostaglandin agonist (PPA). The slope of the PPA aggregation curve decreases with aspirin inhibition and is a sensitive measure of the amount of aspirin induced platelet inhibition (Schwartz J. Lab Clin Med 2002;139:227). Light aggregometry with arachidonic acid was used to verify that the patients had or had not taken aspirin. Maximal aspirin induced decrease in platelet function was defined as the difference between the PPA aggregation curve slopes at the 2 time points, off-aspirin and 2-hours post aspirin ingestion. 187 adult subjects (62% male 38% female) divided into four groups were studied, MI patients without diabetes n=98, diabetics with an MI n=41, diabetics without an MI n=9, and normal subjects n=39. Results: Comparisons of the PPA slopes of the 4 groups showed that diabetics had higher slopes than non-diabetics. Platelets from diabetics with and without an MI had significantly (p<0.05) increased off aspirin platelet reactivity (PPA slope) compared to normals. At the 2 hr time point patients with diabetes and an MI had a significantly higher PPA slope than the MI without diabetes group. Maximum aspirin induced decrease in platelet function was negatively correlated with age (r=-0.32, p=0.002). When controlled for age, there was no difference in the maximum decrease in platelet function among the 4 groups. Conclusions: 1. Platelets from diabetic patients with and without MI have increased platelet reactivity to PPA. 2. The maximum decrease in platelet function observed in diabetic patients with and without an MI was similar to that observed in MI patients without diabetes and in normals. This suggests that the decreased protection from future vascular events observed with aspirin in diabetic patients is not because of an intrinsic resistance to aspirin inhibition of platelets. Disclosures: No relevant conflicts of interest to declare.